C63-26 Flash Leukostatic Pulmonary Edema in a Patient With Chronic Myeloid Leukemia and Congestive Heart Failure: A Delicate Balance Between Diuresis and Leukapheresis

Abstract Introduction Chronic myeloid leukemia (CML) accounts for 15-20% of adult leukemias, with an incidence of 1-2 per 100,000 annually and a slight male predominance. Hyperleukocytosis, defined as a white blood cell (WBC) count exceeding 100 × 109/L, can lead to leukostasis—a medical emergency marked by microvascular obstruction and tissue hypoxia. The lungs and central nervous system are most frequently affected, but cardiac and renal complications can be life-threatening. Patients with underlying congestive heart failure (CHF) and CML have notably higher mortality. This case highlights the diagnostic complexity and fluid management challenges in CML-associated hyperleukocytosis complicated by diastolic CHF. Case Presentation An 85-year-old woman with type 2 diabetes, hypertension, severe aortic stenosis status post-transcatheter aortic valve replacement (TAVR), diastolic CHF, paroxysmal atrial fibrillation, and cryptogenic cirrhosis presented with lightheadedness and progressive dyspnea. Laboratory studies revealed WBC 272 × 109/L (7% blasts), uric acid 14 mg/dL, and acute kidney injury (creatinine 1.28 mg/dL; baseline 0.9). Non-contrast head CT and carotid duplex were normal. CT chest/abdomen/pelvis demonstrated bibasilar ground-glass opacities, trace pericardial effusion, splenomegaly, and cirrhotic liver morphology, suggesting combined volume overload and leukostasis. She was treated with IV fluids, allopurinol, hydroxyurea, and rasburicase for suspected tumor lysis syndrome, while home diuretics were held. Initially requiring 2 L oxygen by nasal cannula, her needs escalated to 5 L over 48 hours as respiratory distress worsened. On day 3, she developed acute pulmonary edema; IV fluids were stopped, and she received two 40 mg doses of IV furosemide. Chest X-ray showed significant worsening of pulmonary congestion. Echocardiography revealed EF 60%, aortic valve gradient 12 mm Hg, RVSP 60-65 mm Hg, and a dilated IVC with 50% collapse, consistent with right-sided pressure overload. She was transferred to the Medical ICU for leukapheresis (days 3 and 4). Bone marrow biopsy confirmed chronic-phase CML (4% blasts). After two leukapheresis sessions and continued hydroxyurea, WBC fell below 100 × 109/L, kidney function normalized, and oxygen was successfully weaned off before discharge. Discussion This case underscores the precarious interplay between volume management and cytoreductive therapy in CML-associated hyperleukocytosis. Leukostasis-induced hyperviscosity likely increased afterload and pulmonary pressures, precipitating flash pulmonary edema and secondary pericardial effusion. Imaging and labs often fail to distinguish CHF from hyperviscosity-driven pulmonary compromise. Early leukapheresis, even in chronic-phase CML without blast crisis, is crucial to reverse cardiorespiratory decline. The patient was discharged with outpatient initiation of a tyrosine kinase inhibitor. This abstract is funded by: none